Hello and welcome to the webinar vet and this webinar. My name is Karen grey. I'm a registered veterinary nurse working in the dermatology clinic at the Queen Mother Hospital for Animals, and the aim of this webinar is to guide you on the first steps on working up the pruritic patient.
And pruritus is the terminology used for itch, and it can present in a number of ways that sometimes owners don't recognise as itch. So it could be licking, chewing, scratching, or rubbing. They could be rubbing along the sofa or rubbing their their back along the the grass outside.
And all of these demonstrate ways that we recognise as pruritus. So we have several factors that contribute to prurituss and a process of elimination is required before we rest upon the diagnosis of allergic skin disease, whether that's to the food or or an environmental allergy. The first thing we want to rule out is parasites which cause itch.
Then skin infections such as pyoderma or a yeast infection, which is a microbial overgrowth of the commensal microbes on their skin. And then looking at the error at the bottom of the screen, we also want to recognise and rule out other cases of, or causes of prurituss in the form of skin cancers or autoimmune disorders. So firstly, let's have a look at Parasites.
The most common form of parasitic pruritus is fleas, and most flea infestations go unnoticed. But if the animal has a type one hypersensitivity to a flea bite, it could give quite marked clinical signs. The area of the body affected is most often the dorsum, and you can either see or feel hemorrhagic crusts in that area, a crusted papular rash or millery dermatitis, as it's often called.
And if they're allergic to the flea bite, they can be really potic. And obviously the the the the section I've written at the bottom here is types of areas affected can give us an idea of the issue. So if the dorsum or the flanks are affected, the first thing we think of is usually fleas.
And the dorsum is not a common area associated with allergic skin disease. And cats can really go to town on themselves over grooming any area of the body, not just the dorsum. The initial action we take for poietic cats is robust flea control, as up to 85% of our pruritic cats have fleas, but the owners don't see the fleas, so they often think it's not going to be that.
But because the cat is so itchy, it's grooming all the time and grooming the fleas off and ingesting them. You can see here on the picture on the bottom right, we call the cats head and neck shredders, and this cat needs some glucocorticoids and as as well as robustly controlled, but definitely needs glucocorticoids like prednisolone at 1 to 2 migs per gig a day to reduce the inflammation and the pruritus to, to start to try and heal because these cats will just keep going and really cause damage. So testing for fleas, we perform a coat brush.
And what we do is we rub the dorsum of the animal and collect the scale that falls onto the table. We put that scale onto a slide with liquid paraffin on it, that just holds the debris onto the slide. And cover it with a cover slip and examine it under the lowest lens on the microscope and what we're looking for is what's on the bottom right hand corner, which is these bright ruby red, often curved flea dirt.
These are flea droppings. An itchy animal will likely scratch and cause excoriations in their skin, resulting in scabs and crusts that fall onto the table. And as these are also dried blood, if you do the wet paper towel test, they will also bleed, giving you a false positive.
And that's why we look under the microscope. Also, if we look under the microscope, we, we, we will also find the fermite Kalatella. So that's why we don't tend to do the the paper towel test.
And remember the flea life cycle where the whereby the the female flea after mating will consume 5 times more feed than usual in order to defecate and enrich the environment with sufficient blood droppings to feed the larvae when they hatch. And the eggs and droppings are designed to fall off into the environment and the the larvae eat the flea dirt, the debris, and almost anything else. And incidentally, they will also eat the any tapeworm eggs that have been pooped into the environment.
And once the tapeworm egg is inside the flea's stomach, it relies on the fastidious and itchy cat or dog to groom itself and eat the flea. Whereby the tapeworm is released into the gut of the animal and develops into an adult worm. And then that produces eggs which seed the environment and the process starts again.
So we can confidently tell an owner if the animal has tapeworm, they have fleas. Onto sarcoptes. Sarcoptes is the mite endemic in the fox population in the UK, and dogs, because it's very rare in cats, pick up, pick them up either with direct contact or from the environment whereby the mite can survive for a day or so off of the host.
It causes intense pruritus, as you can see here on the, the bottom left-hand side, our, our dog here in the clinic, it was actually a very nervous dog, but he could not stop himself from scratching. Diagnosis is achieved by taking skin scrapes and examining under the low lens, the fore lens. What happens with sarcoptic mites, the mites get onto the animal, they mate.
The female will then burrow superficially into the epidermis and lay eggs. And the life cycle is only a couple of months long, so she will soon die after that. But the eggs hatch.
They come up onto the surface of the skin to feed. They eat the skin cells and the debris from the host. They mate and the process starts again.
And remember it's zoonotic. So this will be the phone call where the owner calls the surgery and says my dog just won't stop scratching. And unfortunately, this won't resolve itself.
If you don't treat the condition, they just get worse and become really quite, quite miserable. Skin scraping is only 60% diagnostic. And what you can do if you are concerned it's sarcoptes, you would just treat them with something like an isoxazole, preferably something in tablet form rather than a spot on, to ensure penetration.
Apart from the intense pruritus and the ragtag look to the animal on closer inspection, you may see these little yellow crusted papules on the skin, and that's also indicative of a sarcoptic infestation. And you can also do the pinna pedal rub test where if you rub the ear pinna, the dog will attempt to scratch with their leg. This is actually 60% diagnostic.
Demodex is a commensal mite which is passed from the mother to the puppy whilst nursing, and it tends to proliferate if the immune system is compromised in some way. For example, a young bitch that comes into season or an old dog on chemotherapy, the immune system just dips and the mites proliferate. On the top right hand side, you can see the mite dwells quite far into the dermis, so we tend to perform a hair plucking rather than a deep skin scrape, although I'm aware that diagnosis can be achieved with both.
And students often ask, considering the m is commensal, how many mites would suggest acariasis. And there are guidelines on this which suggest if you see one mite, then take more samples. If you see more than one mite, it could be classed as acariasis.
Classic signs of dermatocosis are blocked follicles and follicular casting due to the nature of, of where they reside. And in this photo you can see the commodones, which is the term used for a blackhead. If you plucked the hair, you would just, you'd get a little bit of a follicular casting on the end of the hair, debris at the root of the hair and that's what we call follicular casting.
And we take a hair pluck. Pop it on a slide with liquid paraffin on which just holds the the the hair to the slide, cover it with a cover slip. Look at it under low lens, and this is what you find in the bottom left hand corner.
And I have noticed that different breeds can have certain looks to them when they have dermatocosis, with many bull breeds having either red mange as demonstrated in these photos on the left, and the long-haired breeds may present with crusting. Incidentally, blue mange was often spoken about when I was in general practise, and that's very similar to the images on the left. But rather than the stark erythema that you can see here, because the skin has become chronically inflamed, it's developed hyperpigmentation, which is the blue effect.
And please make note that any chronic podo dermatitis cases should always be checked for Demodex. And different species of demodex can affect cats, but they tend to be on the surface of the skin, and they're extremely potic and also quite rare. A quick reminder about the use of your microscope while you're looking for parasites, and that is to remember to lower the condenser to achieve contrast in your samples in order to see the mite.
So as you can see, the picture on the top right is with the condenser lowered, the light's not particularly high, and that's giving us the shadows and the contrast so we can see these little critters. Whereby the picture on the bottom right hand side we have the microscope set up for cytology, so we want a high condenser and we want a bright light. But as you can see, if you set the microscope up this way, you just don't see the mites.
You don't have those shadows. So always remember to drop your condenser. Coming to the second main causes of prurituss to tick off, and that is skin infection.
These are gonna be our commensal microbes on the skin, our yeast and bacteria that have just proliferated for, for whatever reason that will come to and causing pruritus. So here we have Percy. Percy came to us extremely poetic and really quite miserable, and as you can see here, his skin has been so inflamed for so long.
Not only is it erythematous because it's been chronically inflamed, it's now become hyperpigmented and lichenified, so it's turned black and it's become thickened and leather leathery. So he presented, as we say, with, with pruritus. And his clinical signs were really quite severe with the ventral neck being affected and the local lymph nodes were enlarged.
And that's two indicators of a yeast infection. The ventral neck and, and the local lymph nodes being enlarged. Demodex can also cause enlarged lymph nodes.
But in this case, we took some tape cytology and It was malacesia. It was a yeast, yeast infection. So how did we diagnose that yeast infection?
We, we sampled the surface of the skin. And that involves placing some sellotape onto the onto the skin in a repeated fashion, about 5 taps on the skin to stick the stick to the corneocytes, those dead flaky skin cells that just come off if you, if you rub your skin. We then took the the sellotape and stained it in some diff quick stains and had a look under the microscope.
And this is called tape cytology. And examining the sample on the oil immersion reveals a yeast infection. So here we have our yeast at the bottom, bottom right hand picture here.
The top right hand picture is also yeast, but these are sort of ghost cells of yeast and because yeast causes quite a severic condition very often it's the stains fail to stain them very well, and you really have to look closely to find the yeast. OK, so what did we do with Percy? Well, Percy came to us on Apaquel and malaceb washes, and although Malaceb is indicated for malacisia conditions, because his skin signs were so severe, we really felt that he needed something by mouth.
He needed an oral tablet to get into the system to treat the infection. So we gave him some itraconazole, which is an anti-fungal by mouth every day for 4 weeks. And when he came back to us, he was looking like this.
So he's lichenification and hyperpigmentation was greatly reduced, but now we can see that the the the erythema is starting to come through. So he's despite treating the infection, he's still got a trigger there that's causing his skin to be red and inflamed. Although we had, we'd stopped the Apaquel just to keep things simple, it was quite clear that he needed something for the pruritus, which Apaquel addresses.
But what Apaquel doesn't address is the inflammation. So we switched the Apaquel to glucocorticoids like prednisolone at 1 mg per gig. And, and gave him that for a couple of weeks and we'll see what he looks like on his checkup.
And here we have his 12 week recheck and his hair is growing back. He's not as poietic. He did, however, in the meantime, develop a pyoderma, and we know by Favre's criteria of allergic skin disease that recurrent secondary skin infections like a yeast infection or a pyoderma can be indicative of an allergic.
Skin disease. And so, we treated him for the pyoderma and we concluded that he probably had an allergy to something, so which is causing the secondary infections. So we started him on a workup for allergy.
Of course, we know that our our pyodermas or our our secondary skin infections can also be caused by an endocrine factor like hyperthyroid disease, but in this case with Percy, it was allergic skin disease that was giving him the secondary infections. So microbes love to flourish in skin that doesn't tend to see the air too much, so it'll be our baggy folded dogs like bassets that have those real wrinkly skin. The intertrigo, where the skin rubs together and the microbes have the warm moist places where they can flourish.
We might also see a microbial overgrowths in our facial folds of our bracky dogs or our pendulous ear dogs like the spaniel here in the picture. Or dogs that like to swim and that the skin is kept moist and wet. And here on the bottom right with this pore, this erythematous skin on the pore, we're going to do some tape cytology and we expect to find an overgrowth of of bacteria or yeast.
Coming to another skin infection we often see pyoderma. This presents with pruritus and often a moth-eaten look to the coat, especially on short-haired breeds, and on closer examination reveals epidermal colorettes, rings of erythema with scale, which are remnants of burst pustules that you can see here on the left hand side picture. This is a classic sign of pyoderma, a skin infection.
And it's usually due to an overgrowth of the animal's own bacterial flora, such as Staphylococcus pseud intermedius on dogs. And as I said before, pyoderma can result from either allergic skin disease, endocrine issues, or can be an isolated incident. Fleas, for instance as well can cause sort of hotspots and and set off a pyoderma.
And pyoderma can have several stages to it, as we can see in the pictures at the bottom, it can start off with a papule, a small red bump that develops into a pustule. And then as that bursts, it leaves this epidermal cholera. And we can take tape cytology of any of these stages and get our diagnosis.
So we could take a tape impression of the papule or the epidermal colorette, or we can burst the posture with a needle and press a slide against it for an impression smear. And stain these samples up and have a look under the, under our oil lens and this is what we'll find, we'll find out our neutrophils, phagocytosine, our cocci bacteria. So in summary, skin can become diseased through many processes and the clinical history can be informative for diagnosis, such as our, our dog that might have been hanging around a fox den for sarcoptes or the location and the appearance of the skin lesions can provide clues about the underlying condition.
Just like our our dorsally affected itchy cats is likely to be fleas more than allergy. And basic tests can aid diagnosis. You can see that the tests are easy to do, that they seem to be relatively cheap by comparison.
And they're non-invasive. So a process of elimination really is required before we go jumping to our allergic skin disease diagnosis and putting these dogs on lifelong allergy drugs. OK, and onto our allergic skin disease.
OK, so we've ruled out our parasites causing pruritus and our skin infections, and yet the animal is still coming back to you, erythematous and itchy and inflamed, and we can come to a diagnosis of an allergy. And allergies can be broken down further. They could either be a an allergic reaction to a flea bite.
We, we covered that in, in parasites. If they're allergic, they, they can really cause distress, whereas most animals with fleas, you may not notice, or they can be allergic to the proteins in the food or an environmental allergen. So what is atopic dermatitis?
It's a a prevalent multifaceted pruritic skin disease. It's non-curable and that has a detrimental impact on the quality of life of affected animals and their owners. Considering patients' quality of life, response to therapy, potential adverse effects, owner compliance and medication costs because we're going to be treating this, these animals for life.
It's genetic in origin and it's an immune dysregulation in the skin of atopic dogs that leads to the overproduction of pro-inflammatory mediators and that cascade of events leaves the skin inflamed and pruritic. And as I said, it is genetic in origin, so we do advise not to breed from bitches or sires that have atopic dermatitis. The body's response to pathogens.
Allergen presenting cells are dendritic cells that reside in places of the body where antigens are most likely to occur, so the skin, airways, and the GI system. The dendritic cell that sits in the skin is called a Langerhan cell. Allergen presenting cell's job is to collect pieces of foreign antigen and present it to the immune system, and depending on what cytokines are released is what the immune system does.
Essentially they, they ask the immune system, how should we respond to this? IL 31 is one such cytokine released, and that is what medications such as oplacitinib and Lyvemab work on. They block IL 31, thus stopping the itch pathway.
However, they do not stop inflammation. To address inflammation, in particular with otitis, glucocorticoids would be the more indicated. As we know, the ear canals are surrounded by cartilage, so they cannot swell outwards when inflamed.
They can only swell inwards and become stenosed. So an anti-inflammatory is the preferred choice to reverse stenosis associated with otitis. And with atopic dermatitis, what happens is the dendritic cell picks up the antigen invader and presents it to the immune system, the T cell, and depending on what cytokines are released, as we know the immune system responds, let's say for example, IL-4 cytokine is released, and what that does is it raises the body's temperature to try to burn off the pathogen.
Or the T cell may instruct more neutrophils to flood the area, to fight the infection. And due to the immune dysfunction in atopics, the T cell instruct the B cells to overproduce IGE, and they sit on the mat cells, and when they're pre-exposed to the allergen, they degranulate, causing edoema of the vessels that attracts more neutrophils to the area, creating heat and inflammation, and that causes itch. So there is a criteria that we use to determine atopic dermatitis, and that's called Favro's criteria.
And usually we see that the onset of inflamed and ritic skin happens between 6 months and 3 years of age. Their front feet are affected mostly but very often all of their feet are affected, but in Favre's criteria, the front feet are affected. They have a steroid responsive pruritus.
They have a history of recurrent pyoderma or malacisia skin infection. The pinnae are affected, not the pin or margins that will be your sarcoptes. The dorsum is not affected, that's likely to be fleas.
And they have pruritus without the skin lesions first to explain it. First of all, they are just itchy and red. And indeed we have predilection sites for atopic dermatitis, and we can see that in this picture here.
And very often we will have our dogs with chronic otitis, repeated ear infections. It's very often driven by an allergy. And likewise with our dogs that scoot their bottom along the floor.
It could, it could also be if, if it's not anal sacs disease or or worms. We could be looking at the reason that they're scooting in fact, is the skin around the anus is itchy and that's why they're scooting. And they present in these signs with erythema.
They may have a little papular rash if the, if it's been going on for a while, the these areas could be hyperpigmented or lichenified. And they could be chewing, nibbling their feet, or they could have, as I say, repeated cycles of otitis. Clinical signs, as I said before, it's erythema.
It can lead to hyperpigmentation and lichenification if it's left unchecked. We may get a papular rash and the inflamed skin leaves the body susceptible to secondary microbial infection. And there is evidence that dogs with atopic dermatitis do have epidermal barrier abnormalities, including abnormal lipid and ceramide composition, and that results in dry skin due to the increased transepidermal water loss and increased penetration of allergens into the skin.
And they also have an enhanced susceptibility to irritants and infections, and that contributes to the disease severity. So we get a lot of our secondary microbial infections. Bacterial and yeast infections are common in atopic dogs due to increased colonisation of Staphylococci, reduced production of antimicrobial peptides by epidermal cells, and hypersensitivity to their own microbial flora.
What are they allergic to? Well, if they're allergic, if it's an environmental allergy, they could be allergic to the dust mites, the storage storage mites, any mites that are in the environment, tree pollens, grass pollens, feathers, if they're sleeping on the beds or living near a farm, cat epithelium moulds, and, and many more that we test them for. And if there is a food allergy, it could be an allergy to the proteins in the food.
Well, here's our familiar slides. We've got our poietic animal and we've ruled out the other two factors. We've come to the diagnosis of allergy.
So now we're going to determine whether it's a an allergic trigger is the food or whether it's an environmental allergy. And we're also, as we're doing this, we're going to maintain good flea control. So to differentiate between food induced and non-food induced atopic dermatitis, a diet trial is performed, and I really want to stress that this is a diagnostic test.
We don't just put the animal on this hypoallergenic food and leave them on it. The trial lasts 8 weeks to determine if the animal has a food allergy. Antipyretic medication is withdrawn 6 weeks into the trial.
To avoid masking pruritus, and if the pruritus and inflammation resolved by the end of the trial, the food is likely the cause. And to confirm this, the animal is reintroduced to its original diet to induce a flare. If there is no response to the diet and the skin issue persists, an environmental allergy is likely.
Is it a local microbial overgrowth or is it atopic dermatitis? Atopic dermatitis is an inside out disease characterised by generalised inflammation in these predilection sites. And in contrast, local microbial overgrowth, such as in trigo or where the where the skin folds sit together without air circulation leads to localised inflammation and infection.
For example, the picture on the left likely shows a local infection affecting only two toes, whereas the picture on the right shows the entire foot is affected, indicating a more generalised condition, and local infections can often be managed with topical washes or medications. So we've got our diagnosis now, which was a process of elimination. You'll notice that the diagnosis is made in the consulting room.
There is no allergy test, as such to, to diagnose atopic dermatitis. And now we've diagnosed it, we're gonna see how we manage it. The importance of flea control, so evidence exists that atopic dogs are predisposed to hypersensitivity reactions when exposed to flea salivary antigens.
Therefore, all dogs with atopic dermatitis should receive year-round flea preventatives. And despite their extensive use in practise, there is insufficient evidence for the use of antihistamines. Sometimes we find that they might actually just sedate the animal stuff and scratch in that way, but they're not, not really causing any antipyretic.
The therapeutics. Management often involves immune modulators such as cyclosporin or glucocorticoids like prednisolone to suppress overactive immune inflammation. The approach to managing chronic disease is similar to that for acute flares.
Identifying and correcting triggering factors is crucial. If we have an animal that's previously been diagnosed at atopic dermatitis and has been quite happy for months and months on medication and suddenly has a big flare, rather than it could be that a change of season, with, with different antigens that are coming into effect. But rather than keep going up and up and up on our medication if it's not working, go back to basics and just make sure that they, there's no parasitic infection or or skin infection muddy in the waters of our allergic control.
Ciclosporin suppresses the circulating surveillance T cells that are responsible for managing tumour cells. So we sometimes see hyperplasia along the gum line. So be careful to check this area.
And unfortunately, the medication needs to be withdrawn if this happens. Glucocorticoids such as prednisolone works wonderfully on inflammation and pruritus, and since nearly every cell in the body has receptors for steroids, that's also why they work so well, and that's why we get the side effects on long-term therapy. In this clinic, we, we try to go with the lowest frequency as possible, every other day dosing or a couple of times a week dosing if possible, rather than the daily steroids which can give us those nasty side effects.
Steroids are manufactured by the adrenals naturally in the body, and they make the adrenals may atrophy. If we are supplementing the body with extra steroids, which is why we taper them before stopping suddenly, it just allows for the adrenals to wake up and stop producing themselves. Otherwise, we may stop them too suddenly and the animal may go into shock.
Olacitinib and Loyvemab are great for when the animal's inflammation is managed and there is no secondary infection, but they're not often a very good place to start on. They're more maintenance therapy, I think, once everything is settled, or if it's just a mild, mild disease. We can improve the cutaneous barrier by giving oral essential fatty acids, moisturising shampoos and sprays, and we manage the secondary microbial infection as often as possible with topicals or shampoos rather than oral antibiotics.
What we need to do is wet the animal all over, apply the shampoo on as neat as possible, rub it in and leave it on for 10 minute contact time and then rinse. And we may ask the owner to do this several times a week. Management strategies of allergies, well, avoidance would, would be great, especially if it's a a food allergy.
We can manage it with diet alone. Unfortunately, only 10 to 20% of dogs have a food allergy. Integrated pest management, if it's a flea allergy, and if it's a non food induced atopic dermatitis, and that's managed with reducing the inflammation on the skin, managing secondary infection whilst promoting good skin barrier health.
And alternative management strategies involves performing a skin test where we sedate the animal and inject a small amount of potential allergens under the skin to see what causes a wheel and flare and then formulate a crude extract of that allergen. And then inject subcutaneously into the animal, escalating doses of the allergen that gradually decreases the IGE dominated response. But it does only work with about a third of patients unfortunately.
And we will try the immunotherapy for up to 1 year before we decide if it's working or not. Other management strategies could be our Loyvetmab and our Apaquel, our lacitinib. Incidentally, Loyvetmab is a mouse protein mixed with a dog protein.
So sometimes what happens it's working quite nicely for a couple of times and then suddenly the dog's immune system recognises that it's a foreign mouse protein and it starts to make antibodies against it and it just stops working. And obviously it must not be given to cats. And cats exhibit similar hypersensitivities to dogs but may display them differently, including respiratory or gastrointestinal signs or cutaneous signs of feline allergic skin disease.
They may be allergic to flea bites, food proteins, or environmental antigens. And cats can cause significant self trauma as you show, as I showed you in the photos earlier in the presentation, with their sharp claws and their barbed tongues, and management often involves glucocorticoid therapy at 1 to 2 mg per day, reduced once the pruritus resolves, and we give them good flea control. And that concludes this webinar.
I do hope you enjoyed it. Please work your way through the questions attached to this webinar to gain your CPD certificates, and many thanks and good luck in your dermatology.